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Immunological aspects of type 1 and 2 diabetes mellitus.

Lernmark, A. LU orcid ; Baekkeskov, S. ; Gerling, I. ; Kastern, W. ; Knutson, C. and Michelsen, B. (1985) In Advances in Experimental Medicine and Biology 189. p.107-127
Abstract

IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells.... (More)

IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells. Similar phenomena may be observed in patients initially diagnosed as NIDDM and treated with oral hypoglycemic agents. It has been speculated that these patients have a retarded form of IDDM. It is possible that the combination of specific Class II antigen molecule(s) and an invading antigen (virus, bacterium, chemical etc.) presented to the immune system triggers the formation of effector cells such as B lymphocytes and cytotoxic T lymphocytes which also cross-react with the pancreatic B cells. Multiple exposures to this or related antigens throughout several years may eventually lead a sufficient loss of pancreatic B cells to cause insulin dependence.

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Please use this url to cite or link to this publication:
author
; ; ; ; and
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
host publication
Comparison of Type I and Type II Diabetes : Similarities and Dissimilarities in Etiology, Pathogenesis, and Complications - Similarities and Dissimilarities in Etiology, Pathogenesis, and Complications
series title
Advances in Experimental Medicine and Biology
editor
Vranic, Mladen ; Hollenberg, Charles H and Steiner, George
volume
189
pages
107 - 127
external identifiers
  • pmid:4036712
  • scopus:0021783009
ISSN
0065-2598
ISBN
978-1-4757-1852-2
978-1-4757-1850-8
DOI
10.1007/978-1-4757-1850-8_7
language
English
LU publication?
no
id
f5712ceb-f15c-483d-a345-de704240795c
date added to LUP
2019-09-16 12:39:31
date last changed
2024-03-13 08:23:08
@inbook{f5712ceb-f15c-483d-a345-de704240795c,
  abstract     = {{<p>IDDM occurs predominantly among individuals being class II antigen HLA-DR 3 and/or 4 positive, while NIDDM is not associated with HLA-D. Although the HLA-DR 3 or 4 specificities are prerequisites for IDDM to develop, their high frequencies (about 60%) in the background population preclude tissue typing as a predictive test, underlined by the observation that less than 50% of monozygotic twins are concordant for IDDM. The presence of a number of immune abnormalities argues that the causes of IDDM may be sought in an altered immune reaction against antigens present in the pancreatic B cells and/or in the environment. The majority of IDDM patients of short duration show both cellular and humoral autoimmunity against the pancreatic B cells. Similar phenomena may be observed in patients initially diagnosed as NIDDM and treated with oral hypoglycemic agents. It has been speculated that these patients have a retarded form of IDDM. It is possible that the combination of specific Class II antigen molecule(s) and an invading antigen (virus, bacterium, chemical etc.) presented to the immune system triggers the formation of effector cells such as B lymphocytes and cytotoxic T lymphocytes which also cross-react with the pancreatic B cells. Multiple exposures to this or related antigens throughout several years may eventually lead a sufficient loss of pancreatic B cells to cause insulin dependence.</p>}},
  author       = {{Lernmark, A. and Baekkeskov, S. and Gerling, I. and Kastern, W. and Knutson, C. and Michelsen, B.}},
  booktitle    = {{Comparison of Type I and Type II Diabetes : Similarities and Dissimilarities in Etiology, Pathogenesis, and Complications}},
  editor       = {{Vranic, Mladen and Hollenberg, Charles H and Steiner, George}},
  isbn         = {{978-1-4757-1852-2}},
  issn         = {{0065-2598}},
  language     = {{eng}},
  month        = {{01}},
  pages        = {{107--127}},
  series       = {{Advances in Experimental Medicine and Biology}},
  title        = {{Immunological aspects of type 1 and 2 diabetes mellitus.}},
  url          = {{http://dx.doi.org/10.1007/978-1-4757-1850-8_7}},
  doi          = {{10.1007/978-1-4757-1850-8_7}},
  volume       = {{189}},
  year         = {{1985}},
}